Evidence map›Paper›PMID 28765520›Full record

ArticleNature communications2017

Semaphorin 4C Plexin-B2 signaling in peripheral sensory neurons is pronociceptive in a model of inflammatory pain.

Eszter Paldy, Manuela Simonetti, Thomas Worzfeld, Kiran Kumar Bali, Lucas Vicuña, Stefan Offermanns, Rohini Kuner

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.3field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  8. Keratinocyte-Derived Exosomes in Painful Diabetic Neuropathy.bioRxiv : the preprint server for biology · 2024
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  10. Review
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  16. Identifying Function Determining Residues in Neuroimmune Semaphorin 4A.International journal of molecular sciences · 2022
    Article
  17. Article
  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Eszter PaldyInstitute of Pharmacology, Heidelberg University, Im Neuenheimer Feld 366, Heidelberg, 69120, Germany.
Manuela SimonettiInstitute of Pharmacology, Heidelberg University, Im Neuenheimer Feld 366, Heidelberg, 69120, Germany.
Thomas WorzfeldInstitute of Pharmacology, Marburg University, Karl-von-Frisch-Straβe 1, Marburg, 35043, Germany.
Kiran Kumar BaliInstitute of Pharmacology, Heidelberg University, Im Neuenheimer Feld 366, Heidelberg, 69120, Germany.ORCID http://orcid.org/0000-0002-9503-1402
Lucas VicuñaInstitute of Pharmacology, Heidelberg University, Im Neuenheimer Feld 366, Heidelberg, 69120, Germany.
Stefan OffermannsDepartment of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Ludwigstrasse 43, Bad Nauheim, 61231, Germany.
Rohini KunerInstitute of Pharmacology, Heidelberg University, Im Neuenheimer Feld 366, Heidelberg, 69120, Germany. rohini.kuner@pharma.uni-heidelberg.de.
Heidelberg University · DEMax Planck Institute for Heart and Lung Research · DEPhilipps University of Marburg · DE

Funding

European Research Council
6 · The paper itself

Abstract

Semaphorins and their transmembrane receptors, Plexins, are key regulators of axon guidance and development of neuronal connectivity. B-type Plexins respond to Class IV semaphorins and mediate a variety of developmental functions. Here we report that the expression of Plexin-B2 and its high-affinity ligand, Sema4C, persists in peripheral sensory neurons in adult life and is markedly increased in states of persistent pain in mice. Genetic deletion of Sema4C as well as adult-onset loss of Plexin-B2 leads to impairment of the development and duration of inflammatory hypersensitivity. Remarkably, unlike the neurodevelopmental functions of Plexin-B2 that solely rely on Ras signaling, we obtained genetic and pharmacological evidence for a requirement of RhoA-ROCK-dependent mechanisms as well as TRPA1 sensitization in pronociceptive functions of Sema4C-Plexin-B2 signaling in adult life. These results suggest important roles for Plexin-B2 signaling in sensory function that may be of therapeutic relevance in pathological pain.Semaphorins and their receptors are involved in neurodevelopment, but their functions in the adult nervous system are not fully understood. This study finds that semaphorin 4C and its receptor Plexin B are expressed in sensory neurons and are pronociceptive in a mouse model of inflammatory pain.

Indexed as

InflammationNociceptionAnimalsDisease Models, AnimalMiceNerve Tissue ProteinsPainReceptors, Cell SurfacerhoA GTP-Binding Proteinrho-Associated Kinasesrho GTP-Binding ProteinsSemaphorinsSensory Receptor CellsSignal TransductionTRPA1 Cation ChannelNerve Tissue ProteinsPlxnb1 protein, mousePlxnb2 protein, mouseReceptors, Cell SurfacerhoA GTP-Binding ProteinRhoA protein, mouserho-Associated Kinasesrho GTP-Binding ProteinsSema4c protein, mouseSemaphorinsTRPA1 Cation ChannelTrpa1 protein, mouse

Identifiers

PMID28765520
PMCPMC5539317
OpenAlexW2737761507

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.